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154 Cards in this Set
- Front
- Back
OA is Degeneration of this
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degenerative changes of articular cartilage
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These cells play a role in OA
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Marginal osteophytes
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What age is most affected by OA
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Age > 40 years
> 80% over 75 years old Female > Male In those >65 years, symptomatic 11% knee, 5% hip |
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Primary Cause of OA is
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Majority is Idiopathic
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What are the secondary causes of OA
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Congential disorders
Metabolic disorders-Hemachromatosis, Crystal deposition diseases |
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Apart from the primary and secondary causes of OA what are the other causes?
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Post-Traumatic and Post-Surgical OA
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Congential disorders that can cause OA
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SCFE, congenital hip dislocation
Mechanical features leg-length discrepancy Varus/valus deformity Scoliosis |
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W are the risk factors for OA
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Obesity – knees
Occupational – bending, carrying heavy loads Sport activity Heredity – DIPs |
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What clinical features would be seen in OA
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Slow onset
Morning stiffness less than 30 minutes, if present Gelling Pain in involved joint Bony joint enlargement Crepitation Effusion possible Typically no soft tissue swelling |
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Is there any diagnostic lab for OA
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No, synovial fluid evaluation can differentiate nature of effusion
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What would U see on an X-ray for OA
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X-Ray evaluations
Bony spurs – osteophytes Subchondral sclerosis, Subchondral cysts Joint space narrowing – Knees - Consider weight bearing view |
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Tx for OA can include
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Conservative Tx: Regular exercise/muscle strengthening, Weight loss
Physical therapy, Splinting- CMC spica, supportive braces and unloading |
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Pt’s OA Sx can be relieved w/
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Symptomatic relief: Topicals OTC
Hot/cold creams – menthol based Capsaicin, Methyl salicylate, Paraffin baths for hand OA |
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What's the 1st line and 2nd line tx for OA
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First line: Acetominophen
Second line- Oral NSAIDs, Topicals -prescription Gels, patches |
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Tramadol can be used in OA when?
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As a non-opiate medication option, eg tramadol
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Other tx, besides NSAIDS and Tramadol, for OA include
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Local treatments:
Intra-articular Injection, Corticosteroids, Viscosupplementation Opiates Surgery |
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What is the indication for Viscosupplementation in OA
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Indication:
Relief from/ to avoid NSAID use Inadequate response to NSAIDs and topicals, and injections Delay surgery |
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These two meds can be used to treat individual joints like the hip, and knees in OA
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Hyaluronan and hylan (HA)
Knees, some recent study of efficacy in the hip Typically have longer effect versus IA steroids |
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What caution should be noted with using Hyaluronan and hylan for OA?
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Allergy to birds, feathers, and eggs
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What are the risk factors for RA
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Genetics, Smoking and Other environmental factors
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rheumatoid arthritis is diagnosed when..
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Morning stiffness lasting at least 1 hr
2. Soft- tissue swelling or fluid in at least 3 joint areas simultaneously 3. At least one area swollen in a wrist, MCP, or PIP joint 4. Symmetric arthritis 5. Rheumatoid nodules 6. Abnormal amounts of serum rheumatoid factor 7. Erosions or bony decalcification on radiographs of the hand and wrist least 4 of these 7 criteria are present, and criteria 1 to 4 are present at least 6 weeks |
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How does RA manifest in the hands?
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Second and third MCP synovial thickening /synovitis
Pain on squeeze of the MCPs Secondary carpal tunnel, ‘boxers gloves’ Triggering secondary to tenosynovitis Decreased grip Boutonniere's and swan neck deformities Ulnar deviation MCP subluxation |
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Other manifestions of RA (apart from the hands) include
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Profound fatigue
Sleep disturbances secondary to pain Early may not be symmetric Occasionally recurrent oligoarthritis Palindromic – relapsing/remitting periods of stiffness/joint pain May present with joint pain, periodic low grade fevers |
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X-ray of your RA hand would show
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Periarticular soft-tissue swelling
Juxta-articular osteopenia Marginal erosions Joint-space narrowing Symmetric involvement Deformities in advanced disease |
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C1-C2 atlantoaxial subluxation in RA is treated how?
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Immobilization collar
Contraindicated procedures/therapy Doing Surgery – fusion Prevents odontoid migration, Cord compression |
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Presence of swan-neck and boutonnière deformity indicates
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Indicates RA
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The progression of RA depends on
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Disease state at time of diagnosis
Ability to induce remission Presence of Anti – Cyclic Citrullinated peptide antibody |
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What are other Non articular related risks/disease associated with RA
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cardiovascular disease
Infection Pneumonitis/ interstitial lung disease Lymphoma Overall decreased life expectancy dependent upon disease progression and control |
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Preliminary evaluation for presence of RA should include
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CBC, LFT CRP, ESR BUN,CRE, Rheumatoid Factor, Anti-cyclic citrullinated peptide (CCP) Antibodies
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What role does the rheumatic factor play
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IgM Antibody to the Fc portion of IgG
Higher levels associated progressive disease Present in approximately 80% of RA patients May be negative in early disease, or in some RA patients May be present in other disorders, both rheumatic and non-rheumatic disease |
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High association with Rheumatoid Arthritis
Indicates a more aggressive course Associated with peri-articular erosions |
Anti –CCP antibody
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Methotrexate (MTX) is a mainstay of treatment
If MTX is insufficient, use combination treatment If failure persists on combination treatment, consider adding a TNF-Alpha inhibitor |
Tx for RA
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Disease Modifying Anti-Rheumatic Drugs (DMARDs) for TX of RA include?
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Corticosteroids, Methotrexate , Hydroxychloroquine, Leflunomide
TNF-Alpha inhibitors Other therapies B-Cell related therapy, Rituximab T cell related therapy, Abatacept IL – 6 inhibitor, Tocilizumab |
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Used in patients who have failed one or more TNF-alpha inhibitors
May be used with or without another DMARD, eg methotrexate |
Tocilizumab
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RA – Remission ACR criteria
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minimum of five of the following for at least 2 consecutive months Morning stiffness not to exceed 15 minutes
No fatigue No joint pain No joint tenderness or pain on motion No soft tissue swelling in joints or tendon sheaths ESR (Westergren's method) less than 30mm/hour (females) or 20mm/hour (males |
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Disease onset <16 years of age
Persistent arthritis 1 or > joints for 6/+ weeks Occurs in absence of other types of arthritis or diseases |
Juvenile Idiopathic Arthritis (JIA)
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This is a subtype of JIA - Mild, may have no swelling, non-systemic
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Pauciarticular
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Complications of JIA include
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Uveitis -May be silent until have vision loss
Frequent eye exams and More common with pos ANA Leg length discrepancies |
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Tx for JIA includes
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Treatment – NSAIDs, IA injection
Exclude joint infection prior to CS injections DMARDs less likely |
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May start similar to pauciarticular, then progress to 5+ joints
Often symmetric knees, wrists, ankles |
Polyarticular JIA
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This is seen as a complication of Poly Articular JIA
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Dactylitis can be present
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Systemic JIA manifests with?
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Quotidian fever
Evanescent/Salmon-colored rash Ill with fever, may appear well when defervesce Koebner phenomenon Arthralgias > arthritis (may present later) |
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What is the TX for JIA's?
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DMARDS
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Quotidian fever can be seen in which type of JIA
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Systemic JIA
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With this JIA The kids are sick! And should r/o infection/hematologic disease
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Systemic JIA
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Labs for Systemic JIA would show
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markedly elevated WBC, Elevated platelets, LFTs and Ferritin, ESR, Anemia
Imaging should also be done |
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Important considerations in Tx of JIA
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Active Inflammatory disease = skeletal damage
May be irreversible if long term Early aggressive treatment needed to quickly control SX/prevent damage RF and Anti-CCP ab are often negative Anterior uveitis frequent monitoring imperative \ Psychosocial issues |
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Tissue deposition of monosodium urate crystals due to hyperuricemicia
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Gout
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What are the manifestations of gout?
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Acute attack
Gouty arthritis Tophi Uric acid nephrolithiasis |
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Hyperuricemia develops due to
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Overproduction of urate (10%)
Ethanol - beer dietary purine precursors G6PD deficiency Myeloproliferative disorders |
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Drugs contributing to hyperuricemia
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Due to decreased renal excretion of urate
Alcohol Loop diuretics – furosemide Thiazide diuretics Low dose aspirin |
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Foods that trigger gout attack
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Purine rich foods
Meats – especially organs Seafood, especially shellfish, sardines, anchovies Vegetables/legumes – asparagus, cauliflower, spinach, beans, peas, mushrooms |
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What crystals are involved with a gout attack
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Crystals are coated with IgG
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Attack triggers for gout
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Acute medical illness, e.g. infections
Trauma Surgery Dehydration/rehydration |
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Clinical symptoms for Gout includes
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Pain, pain, pain
erythema, swelling often lower extremity, 1st MTP or knee Peak pain in hours Self limited - spontaneous resolution days to weeks May involve multiple joints |
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Gout can be Self limited - spontaneous resolution days to weeks T/F
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True
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Labs for Gout include what orders
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Uric acid level: uric acid levels fall during acute attack, Don’t be fooled!
Uric acid level during attack can be in WNL! 24 hour urine uric acid test Evaluation of fluid aspirate X-rays |
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Can be seen on X-rays in gout
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Soft tissue swelling
Tophi Bony erosions “rat bite erosions |
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X- ray for gout show what
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Soft tissue swelling
Tophi Bony erosions “rat bite erosions |
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24 hour urine uric acid test with gout shows what?
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Underexcretion - <800 mg/24h
Overproduction - >800 mg/24h |
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Gout – polarized light microscopy will show what with the crystals?
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Blue in perpendicular and yellow in parallel light
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Uric Acid levels can be low during a gout attack T/F
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True
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What are the indications for tx of Gout
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>2-3 attacks within 1-2 years
Renal stones (Ca or urate) Tophaceous gout Often fingers, olecranon, also larynx, kidney, heart valve, anywhere….. Chronic gouty arthritis with erosions Asymptomatic hyperuricemia? >12 mg/dL or 24 hour urine excretion >1100mg Some rheum recc rx >10….. Hyperuricemia - CV risk |
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Tx of gout
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NSAIDs
Glucocorticoids e.g Prednisone: caution – DM Colchicine: New recommendation : Avoid q hour dosing Require decrease dose in renal insufficiency |
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NSAIDs used in gout Tx
Reversibly inhibits cyclooxygenase Strong anti-inflammatory |
Indomethacin
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Side effects for indomethacin in gout TX
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N/V/D, anorexia, abdominal pain
Frontal headaches, dizziness, Neutropenia, thrombocytopenia |
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Indomethacin, TX for gout, is contraindicated in
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third trimester pregnancy / Category B, not for 3rd trimester or neonates
Black box: CV – increase thrombotic events, MI, Stroke; ulceration/perforation/hemorrhage |
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What can be used for long term tx of Gout
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Colchicine
Xanthine oxidase inhibitors/overproduction 1.Allopurinol 2.Fubuxostat – recent approval Uricosurics /underexcretion 1.Probenecid 2.sufinpyrazone |
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Side effects of Allopurinol, TX of gout?
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Alopecia
Leukopenia GI symptoms Increase risk of attack at initiation/adjustment |
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Uricosurics
1.Probenecid 2.sufinpyrazone TX for Gout causes what side effects? |
Major side effects: rash, GI irritation, hypersensitivity, precipitation of acute attack, and kidney stone formation
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This is asymptomatic or symptomatic
Aka chondrocalcinosis (radiographic) |
CPPD = Calcium Pyrophosphate Deposition Disease
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symptomatic deposition of CPPD in a joint with a subsequent inflammatory response
acute attack May clinically appear similar to Gout |
Pseudogout
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Causes of CPPD
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Idiopathic – majority
Joint trauma Familial – ankh gene mutation effecting pyrophosphate transit channels Aberrant Enzyme NTPPPH, pyrophosphate overproduction |
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Associated diseases that cause Gout
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Hemochromatosis
Hyperparathyroidism Hypophosphatasia Hypomagnesemia Gitleman's syndrome – inherited renal tubular d/o |
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Clinical features of gout
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Typically effects the knee, larger joints
Self limited Pain, stiffness, swelling of the affected joint |
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Systemic manifestation of gout include
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Fever, leukocytosis, ESR elevation.
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What can be used in the diagnosis of CPPD
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Polarized light microscopy of fluid aspirate
Cell count X-Ray Ultrasound |
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Seen on polarized light for CPPD
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rhomboid crystals
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Synovial fluid analysis shows what for CPPD vs OA
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CPPD - Inflammation, Cloudy, yellow
2000-100,000 leukocyte count, decreased viscosity OA- Non inflammatory, clear, yellow and viscous. 200-2000 leukocyte count |
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Responds to steroid tx in CPPD
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Chondrocalcinosis – Knee
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How do you TX Acute pseudogout
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rest joint, consider splinting to protect
1-2 joints - joint aspiration, and IA steroid injection |
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Multiple joints tx in PGout can be tx using
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Oral prednisone, NSAIDs, colchicine
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Chronic (>2 attacks per year) pseudo gout is treated how?
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Colchicine, or if contraindicated, NSAIDs
Joint degeneration is treated as OA |
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This is a chronic inflammatory skin disease. The different types include plaque, guttae, pustular, and erythrodermic. May be associated with inflammatory arthritis.
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Psoriasis
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This manifests with morning pain and stiffness over 30 minutes. Asymmetric arthritis, oligoarticular-DIPs, Enthesitis (inflammation where joints insert), Dactylitis - "sausage digits".
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Psoriatic Arthritis
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The clinical manifestations of this show nail changes - pitting, onchyolysis, transverse ridging. Anteriior uveitis, "Rheumatoid like" disease, other forms can show up with this such as Arthritis mutilans, axial involvement such as poor internal rotation of hips - Asymmetric sacroillitis, and axial syndesmophytes.
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Psoriatic Arthritis
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If you see inflammatory arthritis and a red eye, what can this mean?
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Anterior uveitis which needs an immediate ophthalmology consult.
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What is involved with the axial involvement assocaited with psoriatic arthritis?
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Sacroillitis
Lumbar Spine - Syndesmocytes |
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What diagnostic studies do you order for psoriatic arthritis?
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CBC
ESR, CRP Rheumatoid factor, Anti-CCP antibody NB uric acid Cre, others in consideration of therapy |
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What will be seen on X-Ray imaging with psoriatic arthritis?
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"pencil and cup" appearance of interphalangeal joint.
Erosions Fluffy periosteal bone formation Enthesopathy Sacroilitis Syndesmophytes - asymmetric/coarse |
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What is the TX for psoriatic arthritis?
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NSAIDS
Prednisone Sulfasalazine Methotrexate - don't use with patient who drinks Leflunomide - don't use with patient who drinks TNF-Alpha inhibitors |
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What DMARDS are used to TX psoriatic arthritis?
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Prednisone
Methotrexate - Unsafe/contraindicated for lactation, avoid in patients who drink Sulfasalzine - inhibit prostaglandin synthesis, contraindicated third trimester/lactation safety unknown/avoid, avoid with G6PD deficiency, sulfonamide or salicylate allergy Leflunomide - category X, lactation unsafe, pregnancy should not be attempted for two years after discontinuation TNF-Alpha Inhib. - Etanercept, Infliximab, Golimumab, Adalimumab, inhibition of TNF-A leads to neutralization without cell destruction. |
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What are the major side effects with TNF-Alpha Inhibitors?
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Serious infection
Reactivation of latent TB Reactivation of Hep B Worsening of heart failure |
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This is a non-purulent inflammatory arthritis occurring following infection. Symptoms follow typically a GI or GU infection. Reactive/Reiter's triad shows with this = Arthritis, Urethritis, Conjunctivitis.
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Reactive Arthritis
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The following infections are associated with what?
Bacteria: GI - Salmonella, Yersinia, Shigella, Camphylobacter, Clostridium difficile. GU - Chlamydia, Gonorrhea |
Reactive Arthritis
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This occurs approximately 1-4 weeks following gastrintestinal or sexually transmitted infection. While infection may clear quickly, arthritis may persist for months or become chronic.
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Reactive Arthritis
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This presents with Asymmetric oligoarthritis, Enthesitis - especially in achilles, Dactylitis.
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Reactive Arthritis
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With this you can see inflammatory eye disease - conjunctivitis, anterior uveitis
Mucocutaneous lesions - Balantitis, Stomatitis, Keratoderma blennorhagicum Joint presentations - synovitis/effusion, enthesitis |
Reactive Arthritis
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Keratoderma blenorrhagicum associated with reactive arthritis can show up with a patient who has what disease?
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HIV
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What laboratory evaluations are associated with reactive arthritis?
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Evidence of GI/GU infection via culture (not necessary for diagnosis, but for rx)
Aspiration effusion w/ monoarthritis Fluid studies Cell count, crystals, culture, glucose, consider PCR lyme, chlamydia Urine chlamydia, stool culture |
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What is the TX for reactive Arthritis?
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Treat infection if present
Arthritis may spontaneously remit after 6 months Small percentage persist Treatment is dependent upon severity NSAIDS, local injection If conservative fails/doesn’t resolve, then DMARDs |
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Inflammatory muscle disease
Effects striated muscle Occasionally effects cardiac muscle Can occur with Dermatomyositis Cutaneous involvement Heliotrophe rash, gottron’s papules, shawl (or “V”) sign calcinosis Can be associated with underlying malignancy |
Polymyositis
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Symmetric proximal muscle weakness
Occurs slowly over months Prominent shoulder/pelvic girdle/neck flexors Symmetric proximal muscle pain accompanying weakness May have cardiac or pulmonary involvement Conduction defects ILD May have GI involvement dysphagia/regurg/aspiration Respiratory Diaphragm/chest wall muscle involvement |
Polymyositis
|
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What is involved with the evaluation of polymyositis?
|
Elevated muscle enzymes
CK Others – aldolase, myoglobin, AST/ALT, LDH, myoglobinuria EMG changes Myopathic Muscle biopsy Obtained from weak muscle Usually quad or deltoid Peri-vascular and endomyosial inflammation with fiber necrosis and degeneration These may occur with Dermatomyosis MRI - T2 imaging (fat suppression) for appropriate site guidance |
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What is the TX for polymyositis?
|
Glucocorticoids
High dose initially with goal to taper over 9 months to a year to minimize May require long term medication to spare steroid Azathioprine Check TPMT, thiopurinemethyltranferase - enzyme Methotrexate |
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What do you do to monitor polymyositis?
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Treatment associated side effects
Age related cancer screenings Chest-Xrays - Interstitial lung disease risk |
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A systemic necrotizing vasculitis effecting small and medium sized arteries, that can lead to secondary tissue/organ ischemia.
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Polyarteritis Nodosa - Very Rare
|
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This is associated with hepatitis B
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Polyarteritis Nodosa
|
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The following presentation is associated with what?
Constitutional symptoms Fatigue, weight loss, tachycardia, fever, myalgias, arthralgias Skin Livedo reticularis, nodules, digital ischemia, ulcerations Peripheral nerves Mononeuritis multiplex GI/GU Intestinal angina Mesenteric infarctions or aneurysms Testicular pain Renal Renal and interlobular arteries Microaneurysms, wedge shaped renal infarcts Renin-related hypertension Cardiac Patchy necrosis of myocardium Tachycardia – reflects direct damage or inflammatory state |
Polyarteritis Nodosa
|
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What is the TX for Polyarteritis Nodosa?
|
Glucocorticoids
Localized or systemic Local - Cytotoxic agents –if steroid unsuccessful/inadequate Systemic – Cyclophosphamide Treat Hepatitis B if present |
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What is the side effects of cyclophosphamide, aka cytoxan when given for polyarteritis nodosa TX?
|
Hemorrhagic cystitis
Sterility CI: live vaccines due to immunosuppression Category D; fetal risk, unsafe lactation |
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Can be a "one time" disease where 80% of patients will go into remission after two years.
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Polyarteritis nodosa
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A constellation of symptoms that may include diffuse body pain, sleep disturbance, and depression
“the invisible syndrome” |
Fibromyalgia
|
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The following are associated with what?
"central sensitization" - change in pain perception Abnormalities in sensory processing Stressors – physical/psychiatric trauma Sleep disturbances – apnea, restless legs, obesity Polypharmacy |
Fibromyalgia
|
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The following symptoms are associated with?
General fatigue Anxiety Increased pain in morning, or with anxiety or stress Chronic headaches c/o alternating diarrhea/constipation Subjective swelling or numbness w/o associated objective findings Non-restorative sleep |
Fibromyalgia
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Pain in 11 of 18 tender point sites on digital palpation with approximate force of 4kg. This is associated with what?
|
ACR 1990 Classification Criteria: Fibromyalgia
|
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How is fibromyalgia diagnosed?
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Diagnosis of exclusion - Look for underlying causes
|
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What are the TXs for fibromyalgia?
|
Must treat co-morbid depression/anxiety if present
Maintain activity Treat sleep disturbances Treat depression |
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What is the pharmacotherapy used for fibromyalgia?
|
Tricyclic Antidepressants : Cyclobenzaprine (Flexeril), Amitriptyline (Elavil)
SNRI: Duloxitine (Cymbalta) Anticonvulsant: Pregabalin (Lyrica) |
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Rheumatic disease characterized by acute or sub-acute onset pain and stiffness of the proximal neck, shoulder girdle, and pelvic girdle of at least four weeks duration
|
Polymyalgia Rheumatica (PMR)
|
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More common in Northern European, Scandinavian descent
Associated with Giant Cell Arteritis (GCA) |
Polymyagia Rheumatica (PMR)
|
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Primarily a clinical diagnosis
Acute or sub-acute onset Proximal pain in shoulders, lower extremities, typically symmetric Stiffness of shoulders, hips Absence of objective muscle weakness Exclude physical cause Laboratory testing CBC, ESR, CRP |
PMR Diagnosis
|
|
How do you TX PMR?
|
Prednisone
15-20 mg daily With control of symptoms, commence taper Self-limited, and may be able to taper off completely after 1-2 years |
|
How do you monitor PMR?
|
ESR, CRP, CBC prior to each visit
Monitor for side effects of prednisone Monitor for recurrence of sx as taper May require secondary agent if unable to wean off prenisone without recurrence. |
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What are the signs and symptoms of giant cell arteritis?
|
Signs and symptoms of GCA
Amaurosis fugax / vision changes Jaw claudication Headaches – temporal or other Fever PMR |
|
This is a chronic systemic autoimmune disorder effecting most major organ systems.
|
Systemic Lupus Erythematosus
|
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The pathogenesis of this disease is that it develops auto antibodies causing cell destruction/apoptosis.
|
Systemic Lupus Erythematosus
|
|
What is the main complaint a patient has with SLE?
|
Being tired
|
|
The general symptoms associated with this are as follows:
Fatigue Fever Weight loss Myalgias/Arthralgias Alopecia Rashes Lymphadenopathy |
SLE
|
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What manifestations are seen with SLE?
|
Malar/Butterfly Rash
Interarticular dermatitis Stomatitis Jaccoud's Arthropathy |
|
What pulmonary findings are associated with SLE?
|
Acute lupus pneumonitis - fever, cough, dyspnea, hypoxia, basilar rales, pleural effusion, pulmonary infiltrates on X-Ray, no apparent infection, e.g. negative culture.
Pleural effusions Interstitial lung disease |
|
What is associated with the renal involvement in SLE?
|
Glomerulonephritis - monitor urinalysis for proteinuria and monitor creatinine/GFR
|
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What are the complications associated with SLE?
|
Major cause of death-accelerated atherosclerosis, CV
Renal failure in lupus nephritis Strokes - with positive APL syndrome Opportunistic infections Malignancies - higher risk of cervical dysplasia and carcinoma in females |
|
What is the TX for SLE?
|
Conservative:
Skin - At least SPF 30 sunscreen, topical gluticocorticoids, systemic glucocorticoids Smoking Cessation - Increased risk of flare Treat Hyperlipidemia Avoid Sulfonamides Avoid high dose estrogen |
|
What are the medications used in SLE systemic therapies?
|
Typical Medications - Glucocorticoids, Hydroxychloroquine, Azathioprine
|
|
What immunosuppressive medications do you use in SLE - Systemic treatments/organ involvement?
|
Methotrexate - Arthritis unresponsive to NSAIDS
Azathioprine/Mycophenolate - Mild nephritis, or in remission after pulsed cyclophosphamide Cyclophosphamide - Severe lupus nephritis |
|
This is an episodic, reversible digital skin color change due to vasospasm
Usually cold induced, sometimes emotional distress |
Raynaud's Phenomenon
|
|
This manifests as the following?
Biphasic color changes with cold exposure Symmetric attacks No digital ulcers, pits, or gangrene No PVD Normal nail fold capillary examination Negative ANA and ESR |
Primary Raynaud's Phenomenon
|
|
How do you TX Raynaud's phenomenon?
|
Exclude underlying cause
Conservative - Gloves, mittens, warm clothing, avoid cold exposure, avoid exacerbating medications/substances - avoid caffeine, amphetamine, decongestants (sympathomimetics), smoking cessation Medications - no FDA approved TX, but CCB, Indirect Vasodilator-fluoxetine, phoshodiesterase inhibitor-sildenafil |
|
If you see Raynaud's with late onset over 30 years old, male, ulcerations, pitting, involvement of more than distal digits, involvement of the feet, nail fold changes, laboratory testing abnormalities - ANA, RF
|
Secondary cause of Raynaud's
|
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This is a small vessel vasculopathy that effects small arteries, arterioles, and capillaries causing ischemic reperfusion injury. Proliferation of cells in the intima of small vessels, leading to cascade causing obliteration and proliferative changes - digital ischemia/ulceration, pulmonary hypertension. Increased sensitivity to cold and stress - Raynaud's in 95% of patients.
Fibrosis - Activation of fibroblasts with increased production of collagen, leading to skin thickening |
Systemic Sclerosis
|
|
What are the early manifestations of Systemic Sclerosis?
|
Raynaud's phenomenon
GERD Fatigue Musculoskeletal complaints |
|
Systemic sclerosis is put into what two categories?
|
Limited and Diffuse
Limited - limited to hands, feet and face Diffuse - throughout body, not limited to hands, face and feet |
|
This is a dermatologic presentation of systemic sclerosis seen on the body?
|
En coup de sabre
|
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What diagnostic testing do you use for systemic sclerosis?
|
Anti-centromere antibody
Anti-SCL-70 antibody Nail fold capillary examination |
|
What are the following?
Toxin induced skin changes - vinyl chloride bleomycin organic solvents and resins Vibration injury Eosinophilic fasciitis - cobblestone like skin |
Scleroderma-Like syndromes
|
|
What are the following involved with?
Interstitial fibrosis Pulmonary hypertension Scleroderma renal crisis Digital ulceration/ischemia |
Sequellae of systemic sclerosis
|
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How do you treat systemic sclerosis?
|
No proven disease modifying medication
Treat Raynaud's Watchful waiting/monitoring Treatment of other individual manifestations: Digital ulcers Renal crisis Interstitial lung disease PAH GI disease |
|
What is involved with monitoring systemic sclerosis?
|
Pulmonary function tests at baseline and consider yearly or with change in symptoms.
Echocardiogram at baseline and then annually Chest X-Ray at baseline and then annually BP monitoring Creatinine, Urinalysis Skin Integrity |
|
This is an autoimmune disease involving salivary, lacrimal and exocrine glands. Glands infiltrated by CD4+ T cells, and some B cells. Infiltration by inflammatory cytokines
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Sjogren's Syndrome
|
|
Inflammatory state leads to secretory duct and acinar cell damage. Parotid luminal narrowing, keratoconjunctivitis sicca, GI mucosal dryness and atrophy-dysphagia, vaginal dryness.
|
Sjogren's Syndrome
|
|
What is the clinical presentation of Sjogren's Syndrome?
|
Dry eyes - irritation, photosensitivity, later corneal damage
Dry mouth - tooth decay, candida infections, salivary stones, difficulty swallowing Respiratory tract - dry cough Vaginal mucosa - candida infections |
|
How do you diagnose sjogrens?
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Positive eye tests - Schirmer's test, Rose Bengal Stain, Slit-Lamp examination-Fluorescein
Auto-antibodies - Anti Ro (SS-A), Anti La (SS-B), May have positive rheumatoid factor, may have elevation of ESR |
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What is the TX for sjogrens?
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Conservative:
Regular ophthalmic and dental care Lubricants - Artificial tears/ocular lubricants-hypomellose, methycellulose, gels at night Punctual occlusion Avoid exacerbating issues, eg. contact lenses (soft lenses), and LASIX (contraindicated) Oral - sialogogues - lemon drops, sugar free/alcohol free mouth washes, lubricating gums, gels at night. avoidance of exacerbating substances - Medications - antihistamines, antidepressants, other anticholinergics |